Cryptosporidiosis in Dairy Cattle—Animal and Human Impact
Daryl Nydam, DVM, PhD
Department of Population Medicine and Diagnostic Sciences
College of Veterinary Medicine, Cornell University
Ithaca, NY 14853
Cryptosporidiosis in dairy cattle can be very frustrating to deal with. The agent of this disease, Cryptosporidium parvum, is the pathogen most often diagnosed in preweaned scouring calves (Naciri et al., 1999; de la Fuente et al., 1999). It does not appear to be as life threatening as, for example some serotypes of Salmonella, but under the right group of conditions can cause severe diarrhea and death in young calves (Moore and Zeman, 1991). Clinically affected calves are the most likely animals to shed large numbers of this protozoan, but calves with no outward signs of infection may also shed large numbers of oocysts. In fact, during an infection of average duration, a calf may shed approximately 40 billion oocysts (Nydam et al., 2001). Thus, this pathogen can be very prevalent in the calf’s rearing environment and can be present in the maternity area as well. Reports have estimated the herd level prevalence for fecal shedding in North America ranges from 59-89% (Ruest et al., 1998, Garber et al., 1994).
Calves are primarily infected via the fecal-oral route and it likely takes less than 50 oocysts to infect a healthy calf. The reproductive and infective structure, the oocyst, survives very well in the environment with a portion of the oocysts retaining infectivity after freezing (Fayer et al., 1996). It is also resistant to many disinfectants at farm friendly concentrations, e.g. sodium hypochlorite (bleach) peroxygen (Virkon), and iodophores (Campbell et al., 1982, Ares-Mazas et al., 1997). Six percent hydrogen peroxide and 10% formalin have shown activity against oocysts (Campbell et al., 1982, Weber and Rutala, 2001), but hydrogen peroxide is readily deactivated in the presence of organic matter. The potentially large number of oocysts that survive well in the environment leads to a high likelihood of a susceptible calf being exposed to an infectious dose of oocysts. Once the intestine is colonized, the life cycle of this parasite allows for auto-infection of nearby cells, further decreasing the necessary dose to initiate infection and possibly leading to chronic disease.
The almost constant environmental presence of oocysts, well-adapted life cycle of the parasite, and limited impact of immune enhancement (Harp et al., 1996) often leaves us trying to treat sick calves. Unfortunately, that remains frustrating as well. Many antimicrobial agents have been tried and/or investigated for treating calves with cryptosporidiosis. Among them are allicin, ionophores (monensin and lasalocid), amprolium, decoquinate, sulfas, paramomycin, and halofuginone. Most other antimicrobials have limited pharmacologic basis (e.g. ceftiofur) for use against a protozoan pathogen or are illegal (e.g. metronidazol).
Allicin, a sulfur containing component of garlic, that is available as an additive to milk replacer was shown in a randomized controlled trial not to alter the duration of diarrhea due to C. parvum or enhance weight gain (Olson et al., 1998). Monensin was also found also to be ineffective in an oocyst inoculation trial in calves and rats (Rehg 1993). Lasalocid has been reported to have some efficacy at relatively high doses—5-15 mg/kg (Gobel 1987, Pongs 1989). Unfortunately, this cannot be recommended because doses of 5-8 mg/kg have been shown to be lethally toxic to neonatal calves (Benson et al., 1998). Trimethoprim-sulfa, sulfadimidine, sulfadimethoxine, and amprolium have also been demonstrated to be ineffective against the disease (Moon et al., 1982).
There are many anecdotal reports from the astute practitioners in the field attesting to the utility of a high dose (e.g. 5x) of decoquinate in the prophylaxis and treatment of cryptosporidiosis (AABP-L). In addition, one trial with 5 Holstein bull calves suggested it may reduce the number of days of oocyst shedding and improve fecal scores, but did not prevent shedding of the organism (Redman and Fox, 1993). Unfortunately, in another trial, decoquinate showed little to no activity against the parasite in either cell culture or mice (Lindsey, 2000). The authors of this trial postulated that any apparent clinical improvement of calves with cryptosporidiosis and treated with decoquinate was due to effects other than on C. parvum. The most recent trial examining the effect of decoquinate (Moore et al. 2003) used a dose of 2.5mg/kg (5x label dose) and also did not show an effect of oocyst shedding or clinical signs associated with cryptosporidiosis. This trial did however show that the lower the dose of oocysts received by the calves, the shorter the duration of shedding.
Paramomycin, a human-labeled aminoglycoside, has been shown a number of times to have utility in cell models, rodent models, and is often used as adjunct therapy in patients with cryptosporidiosis and AIDS (e.g. Fayer and Ellis, 1993). A suggested and researched dose in calves is 100mg/kg for 10 days. Unfortunately, this comes with the vagaries of using an aminoglycoside in food producing animals as well as a price tag of about $60/day for a 40 kg calf, i.e. $600 USD. Halofuginone is one antimicrobial that has shown promise in Europe to treat and prevent cryptosporidiosis in dairy calves. In at least 3 trials with reasonable numbers of calves it has decreased oocyst shedding and improved fecal consistency scores (Peters et al., 1993, Lefay et al., 2001, Joachim et al., 2003). Unfortunately, to the author’s knowledge this is currently not available in North America.
In the future halofuginone may become available in North America, but this often takes substantial time (Sanders, 2003). In addition, there has been a recombinant protein vaccine against C. parvum developed that is administered to dry cows somewhat like an E. coli K99 scours vaccine (Perryman et al. 1999). At this point in time it is not commercially available, but it has moved from the research laboratories to pharmaceutical companies for testing.
So now what? The bugs and drugs paradigm often does not work with this pathogen, or most others for that matter, causing scours in dairy calves. Ask yourself, “Can a pathogen that is usually present on a farm be the cause of an increase in disease incidence?” The answer is usually “No”. While Cryptosporidium can cause diarrheal disease in the absence of other pathogens (Heine et al., 1984), usually some other factor in the host (in this case calf), pathogen (in this case Crypto), and environment triad is usually broken also. An example of a host factor is co-colonization with other more virulent enteropathogens, examples of environmental factors include poorly cleaned milk and grain buckets.
So what can we do? Fortunately, most clinically ill calves respond to fluid therapy and supportive care. Remember to watch for metabolic acidosis associated with Cryptosporidium induced diarrhea. Consider supplementing intravenous fluids with sodium bicarbonate1. Be persistent and intervene early with oral electrolyte solutions, while continuing to feed milk or milk replacer at the normal daily rate (divide it into more frequent, smaller feedings if necessary and feasible). Recall the ability of C. parvum to auto-infect adjacent cells and the calf’s slow immune response to the parasite that can lead to protracted disease and necessitates vigilance in care of these calves.
To prevent infection follow best management practices for calves. Be aware that a number of studies have These include removing the calf from the maternity area as soon as possible and putting it in an environment that has been cleaned from previous calf use. Cleaning should include removing bedding and the base (e.g. geotextile fabric or large gravel) and hot water disinfection of the pens. Remember though, that water can spread other pathogens around if it is not used judiciously and the area allowed to dry between calves. As always, wear clean clothes and boots when working with calves.
Cryptosporidium parvum also causes diarrhea and its sequela in a wide range of other hosts including humans by infecting the microvillus border of the gastrointestinal epithelium (Fayer et al., 1997). In humans there have been outbreaks associated with contaminated drinking water (McKenzie et al., 1996), food (Quiroz et al., 2000), and recreational exposure to water (Levy et al., 1998) as well as multiple sporadic cases (McLauchlin et al., 2000). The severity and persistence of cryptosporidiosis is related to the immunocompetence of the host, with the disease being usually self-limiting in those with functional immune systems and life threatening in those that are immunocompromised (Guerrant, 1997). An oddity of human infection is that they seem to have a highly susceptible adult population, whereas most other species acquire some age related resistance.